To summarize the latest advances in PANoptosis-associated mechanisms underlying diabetic retinopathy (DR) pathogenesis and evaluate potential therapeutic strategies.
Approach:
Key Findings:
PANoptosis integrates apoptosis, pyroptosis, and necroptosis, contributing to retinal damage in DR.
Hyperglycemia-induced oxidative stress is a key driver of retinal neurodegeneration.
Current research on PANoptosis in DR is fragmented, with gaps in understanding its mechanisms and therapeutic potential.
Interpretation:
PANoptosis is a dynamic process that contributes to both retinal neurovascular injury and host defense.
Limitations:
Direct evidence of PANoptosome assembly in specific diabetic retinal cell types is limited.
The crosstalk between PANoptosis and immune cell infiltration in retinal inflammation is poorly characterized.
Functional validation of PANoptosis-related genes as biomarkers in DR remains underexplored.
Conclusion:
Future therapeutic strategies should prioritize biomarker-guided, localized, and cell-type-specific modulation of PANoptosis pathways.